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    Tachyphylaxis King PuZo's Avatar
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    Purpose of Glucuronidase Inhibitors?

    What is the purpose of glucuronidase inhibitors such as Calcium D-Saccharate Tetrahydrate? What role does it play in the body?
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    Veritas. Aequitas. neuron's Avatar
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    Originally Posted by PuZo View Post
    What is the purpose of glucuronidase inhibitors such as Calcium D-Saccharate Tetrahydrate? What role does it play in the body?
    Calcium d-saccharate tetrahydrate is a gulcuronidase donor, not inhibitor.

    An inhibitor would block phase II metabolism in the liver, which seeks to make substances more water soluble via conjugation (glucuronidation/sulfation).

    If a drug is determined to be heavily dependent on phase II metabolism, then blocking this step would increase the drugs half-life.
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    Tachyphylaxis King PuZo's Avatar
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    Originally Posted by neuron View Post
    Calcium d-saccharate tetrahydrate is a gulcuronidase donor, not inhibitor.

    An inhibitor would block phase II metabolism in the liver, which seeks to make substances more water soluble via conjugation (glucuronidation/sulfation).

    If a drug is determined to be heavily dependent on phase II metabolism, then blocking this step would increase the drugs half-life.
    So I'm assuming that would be the reason why it would be included?
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    Originally Posted by PuZo View Post
    So I'm assuming that would be the reason why it would be included?
    I mispoke above. It is a glucuronidation donor, and a glucuronidase inhibitor. The end result is the same: decreased half-life of substances heavily dependent on phase II metabolism in the liver. It also blocks bacterial de-conjugation in the gut, which decreases biliary-intestinal re-circulation. The result of this process increases intestinal elimination of various substances.

    OTOH, substances like quercetin or kaempferol decrease glucuronidation, and therefore would prolong the half-lives of substances undergoing phase II metabolism.
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    Tachyphylaxis King PuZo's Avatar
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    Originally Posted by neuron View Post
    I mispoke above. It is a glucuronidation donor, and a glucuronidase inhibitor. The end result is the same: decreased half-life of substances heavily dependent on phase II metabolism in the liver. It also blocks bacterial de-conjugation in the gut, which decreases biliary-intestinal re-circulation. The result of this process increases intestinal elimination of various substances.

    OTOH, substances like quercetin or kaempferol decrease glucuronidation, and therefore would prolong the half-lives of substances undergoing phase II metabolism.
    And quercetin has other benefits as well? Does the glucuronidase inhibition help regulate estrogen levels?
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    Originally Posted by PuZo View Post
    Does the glucuronidase inhibition help regulate estrogen levels?
    One of the main ways through which the body regulates estrogen is via conjugation (phase II), and biliary excretion. Some % of that estrogen is de-conjugated (via bacterial beta-glucuronidase), and reabsorbed. Blocking this event with the previously mentioned substance does indeed lower systemic estrogen levels. The problem with this compound is that it can potentially decrease the half-lives of whatever else you are also supplementing with.
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    Tachyphylaxis King PuZo's Avatar
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    Originally Posted by neuron View Post
    One of the main ways through which the body regulates estrogen is via conjugation (phase II), and biliary excretion. Some % of that estrogen is de-conjugated (via bacterial beta-glucuronidase), and reabsorbed. Blocking this event with the previously mentioned substance does indeed lower systemic estrogen levels. The problem with this compound is that it can potentially decrease the half-lives of whatever else you are also supplementing with.
    And the half life is once it's absorbed by the body? The other main substance would be DAA.
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    Originally Posted by PuZo View Post
    And the half life is once it's absorbed by the body? The other main substance would be DAA.
    Not quite.

    http://en.wikipedia.org/wiki/Biological_half-life

    The biological half-life or elimination half life of a substance is the time it takes for a substance (for example a metabolite, drug, signalling molecule, radioactive nuclide, or other substance) to lose half of its pharmacologic, physiologic, or radiologic activity... In a medical context, half-life may also describe the time it takes for the blood plasma concentration of a substance to halve ("plasma half-life") its steady-state.
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    Tachyphylaxis King PuZo's Avatar
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    Originally Posted by TheWaffleIron View Post
    So it can decrease the total half life of the entire product?
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    Originally Posted by PuZo View Post
    And the half life is once it's absorbed by the body? The other main substance would be DAA.
    After ingestion, it is absorbed via enterocytes and placed in the portal vein. It then circulates to the liver where the majority of metabolism (phase I/II) takes place (first pass).

    You don't want to hear my thoughts on DAA.
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    Originally Posted by PuZo View Post
    So it can decrease the total half life of the entire product?
    Anything predominantly metabolised by phase II metabolism.

    This is mainly determined through urinalysis screening for conjugates vs. plasma metabolites.
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    Originally Posted by neuron View Post
    After ingestion, it is absorbed via enterocytes and placed in the portal vein. It then circulates to the liver where the majority of metabolism (phase I/II) takes place (first pass).

    You don't want to hear my thoughts on DAA.
    I do. Spill it.
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    Originally Posted by adjusting View Post
    i do. Spill it.
    +1!
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    Originally Posted by neuron View Post
    You don't want to hear my thoughts on DAA.

    Let's hear it
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